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CNM Nut2 S2 Exam revision > Ageing MS and Parkinsons > Flashcards

Ageing MS and Parkinsons Flashcards

1
Q

Define Alzheimers?

A

Misfolding of Amyloid beta/Tau proteins. Hippocamal neurons are lost.

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2
Q

Describe the 3 types of alzheimers

A

Hot/Inflammed: M1 + reduced SIRT1. M1-M2 (using nrf2). NFkb increases M1.
Cold Atrophic - reduced BDNF (neuroprotective protein)
Cortical/toxic - linked to environmental toxins - chronic inflamm +brain atrophy.

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3
Q

What is nrf2?

A

a transcription factor supporting shift from M1 to M2 (microglia - resident immune cells of the brain).

It senses cellular stress to increase glutathione enzymes/ SODs/Catalase/ Phase2 detox enzymes

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4
Q

Risk factors for Alzheimers

A

Dysbiosis - via microbiota brain-gut axis - comms to TLR on brain microglia

Oxytoxin: enriched social interactions - through vagus nerve can supress microglia-related inflammation

Oral dysbiosis: P Gingivalis - increased risk of Alzhimers

Aluminium/lead/mercury

Obesity - T2DM stress on body/brain. Pheripheral/neurological inflammation

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5
Q

Diets and natural approach to Alzheimers?

A

MIND (mediterranean + DASH) - mildly ketogenic 12/3.
Medditerranean diet
Coconut oil (MCT rich) -easily absorbed. increase blood ketone + cognitive/brain energy.
Yoga
vagus nerve stimulation
Dietary choline (aceytlcholine for mood/memory/learning)

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6
Q

Supplements and doses for Alzheimers

A

Vit C (mg)
Lactobaccilus Acidiphillus (1-4bn)
CoQ10/B Complex/Vit E
Citicholine (250mg)
Curcumin (500)
Vit D (2000iu)
Omega 3 (750mg)
Reservetrol (100) - protect from misfolded Amyloid

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7
Q

Multiple Sclerosis - what is it?

A

Inflammation of immune cells infiltrate BBB and attack myelin Sheath. Oligodendrocytes reduce (which produce myelin sheath) and neurodegeneration ensues.

T cell mediated - TH17 (away from T-Regs)

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8
Q

Types of MS?

A

Relapse/remitting
primary/progressive
Secondary/progressive
CIS (once)

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9
Q

Risk factors for MS

A

low vit D/K/B12
EBV
Childhood trauma
Mitochondrial dysfunction
Smoke
AI
Toxins
Obesity (BBB permeability - CNS inflammation) Leptin increases TH17. Increased M1 microglias (M2 boosts myelin sheath/oligodendrocytes)
Thymic involution increases autoreactive T cells.
Parasympathetic vs sympathetic state - Autoreactive T cells/myelination

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10
Q

Diets for MS

A

Swank diet (low saturated fat/fruit and veg/ no read meat or pork for 1 year/limited fish and poultry.

Wahls protocol: DGLV/sulphur rich/colourful/Omega 3/grassfed/seaweed

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11
Q

Supplements for MS

A

Vit D/K
Quercetin (500mg)
Alpha Lipoic (300)
Citicholine (250)
Omega 3 (750mg)
B12 (1g)
Methyl folate (500mcg)

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12
Q

Describe Parkinsons Disease

A

Gradula loss of dopamine producing neurons.
Affects substantia Nigra
Misfolded protein Alpha Synuclein - oxidative stress - lewy bodies (aggregate around dopamione neurons) - mito loss/neuron loss, OX stress.

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13
Q

Initial symptoms of PD

A

Constipation and loss of smell

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14
Q

Causes/risk factors of PD

A

Recreational Drugs (esp Amphetamines)
Brain injury/trauma
Mitochondrial dysfunction (Oxidative stress and inflammation)
Toxicity
stress/depression
pesticides/herbicides (Rotenone, paraquat)
Aluminium toxicity. Mangenese/iron/mercury toxicity

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15
Q

Ways to diagnose PD

A

DatScan (Tremors v PD)
PET scan (Brain irregularities)

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16
Q

How does L-dopa act in the treatment of Parkinson’s disease (PD)?

A

L-dopa can cross the blood-brain barrier and is converted into dopamine within the central nervous system, serving as a precursor to dopamine.

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17
Q

What is the role of serotonin neurons in L-dopa medication?

A

Serotonin-producing neurons convert L-dopa to dopamine using the enzyme amino acid decarboxylase. However, L-dopa can damage serotonin neurons, leading to potential negative psychological effects.

18
Q

How does the decarboxylase inhibitor in L-dopa medication function?

A

Prevents the conversion of L-dopa into dopamine outside the brain, ensuring a higher level of dopamine reaches the brain.

19
Q

Why is it recommended to take Vitamin B6 away from L-dopa medication?

A

It may interfere with the function of decarboxylase inhibitors.

20
Q

From where is L-dopa derived, and how can patients benefit from it?

A

Amino acid tyrosine.

Some patients benefit from eating protein-containing meals after their medication, facilitating easier L-dopa passage into the brain.

21
Q

What is the Catecholaldehyde Theory of PD?

A

The theory involves the degradation of dopamine in a neuron’s cytosol to form the toxic compound DOPAL, primarily through the action of the enzyme monoamine oxidase B (MAO B). L-Dopa medication can significantly increase DOPAL levels.

22
Q

How does DOPAL interact with alpha-synuclein in the context of PD?

A

DOPAL interacts with alpha-synuclein, promoting misfolding and the formation of toxic Lewy bodies. Misfolded alpha-synuclein accelerates the formation of toxic DOPAL.

23
Q

What are suggested neuroprotection strategies in PD treatment?

A

Slowing down monoamine oxidase B (MAO B) and promoting the detoxification of DOPAL to its metabolite, DOPAC, for protecting dopaminergic neurons.

24
Q

Other things that can be done for PD patients

A

Hyerbaric oxygen
Avoid EMFs from mobile phones and microwaves
Chelation of Aluminium
Alpha Lipoc acid can chelate iron deposits from brain

25
Q

What protocol can be used for PD patients and Alzheimers?

A

MEND protocols 1 &2
Optimise diet
Exercise/reduce stress
Brain stimulation
CRP test
B5/6/12/folate test
GI health
Glucose optimisatiom/insulin
Vit D optimisation
Synaptic components
Support mitochondria
Check HM toxicity
MCTs (Coconut oil) - brain energy

26
Q

Supplements for PD

A

Vit C (5000)
alpha Lipoc Acid (300)
Taurine (1000mg)
Lactobacillus acidophillus]CoQ10
Citicholine
Curcumin (500)
Vit D (2000iu)
Omega 3 (750mg)
Methyl folate (500mcg)

27
Q

Which berries are MAO-B inhibitors and what toxic compound do they protect against?

A

Blackberry, blueberry, blackcurrant.

Protect against toxic compound- Dopal

28
Q

Describe the mitochondrial theory

A

Mitochondria are the main source of ROS in a cell.
Oxidative stress within mitochondria leads to mtDNA mutations, reduced ATP and energy.
Mitochondrial dysfunction leads to apoptosis (programmed cell death).
Mitochondrial dysfunction is linked to MS, Alzheimer’s and Parkinson’s diseases and many chronic inflammatory diseases

29
Q

hormesis

A

to ‘excite’. How mild stress triggers antiageing reactions in our cells

a process in which exposure to a low level of stress or toxicity induces an adaptive, beneficial effect in a cell or organism.

30
Q

What can mildly stress the body (Hormesis) and how?

A

calorie restriction
phytochemicals
exercise
cognitive stimulation
intermittent exposure to mild cold and heat

By increasing the production of endogenous antioxidants and cellular quality control mechanisms

31
Q

What factors contribute to our allostatic load? How?

A

Exposure to toxins (from the environment, household, cosmetics)
Inadequate exercise
Poor nutrition
High stress levels
Genetic susceptibility
Chronic inflammation
Dysbiosis (microbial imbalance in the body).

↑production of glutathione, catalase, superoxide dismutase and phase II detoxification enzymes.

32
Q

Calorie restriction and exercise - explain effect

A

induce stress partly by depleting cellular energy ↓ATP ↑ADP ↓NADH ↑NAD.

Low cellular energy:

Activates AMPK, a pro-longevity protein.

Activates the sirtuins (SIRT 1-7), a family of anti-ageing proteins.

AMPK and sirtuins initiate a process called autophagy (self-eating), where worn-out or damaged cellular components are digested to improve the quality of the whole organism. Mitophagy (autophagy of mitochondria)

In a healthy cell, mitochondria undergo mitophagy every few days.
Depending on the type of tissue, mitochondria are digested 9-25 days after their biogenesis to maintain their ability to produce energy.

33
Q

Autophagy defends against the 9 key signatures of ageing - what are they?

A

Genome instability.
Telomere shortening.
Epigenetic alterations.
Loss of protein regulation and disposal — a hallmark of Alzheimer’s and Parkinson’s diseases.
Insulin resistance and poor nutrient sensing.
Cell senescence (biological ageing). Stem cell loss.
Altered intercellular communication.

34
Q

How do positive social connections impact health, particularly in older adults?

A

a potent anti-inflammatory factor, comparable to quitting smoking or regular exercise.

35
Q

What is the role of Phase I detoxification enzymes, and what can trigger them?

A

Phase I detoxification enzymes convert xenobiotics, steroids, and drugs into reactive forms with the addition of oxygen. Hydrocarbons from smoked/cooked foods can trigger these enzymes.

36
Q

Why is excessive Phase I detoxification associated with ageing and cancer?

A

Over-activation of the aryl hydrocarbon receptor (AhR) leading to accelerated ageing, cardiovascular disease, and cancer is associated with excessive Phase I detoxification.

37
Q

How do plant compounds support detoxification, and what role does Nrf2 play?

A

Plant compounds induce phase II and III detoxification through anti-ageing Nrf2 activation. Phase II conjugates or binds to reactive intermediates, while Phase III removes detoxified metabolites from cells.

38
Q

What are the key aspects of the Okinawan diet associated with longevity?

A

high in unrefined carbohydrates,
small/moderate amounts of lean meat and fish,
high intake of vegetables/legumes,
low in saturated fats.
eating until 80% full
Small plates

39
Q

How do practices like calorie restriction and intermittent fasting contribute to anti-aging effects?

A

Calorie restriction, intermittent fasting, and fasting activate sirtuins, anti-aging proteins, improving various aspects of health, including mitochondrial activity, cardiovascular health, and DNA integrity. These practices also increase adiponectin, linked to longevity.

40
Q

What are the consequences of obesity on mitochondrial health?

A

Experience mitochondrial dysfunction and reduced biogenesis.

Encounter a loss of viable stem cells, impacting tissue repair and renewal.

Have increased inflammageing, contributing to inflammation. Advanced glycation end products (AGEs):
Proteins modified by glycation can bind to AGE receptors (RAGEs) and induce inflammation.

AGEs are linked to accelerated aging, neurodegeneration, diabetes, and cancer.

41
Q

Name nutrients for anti-ageing

A

B vits
Omega 3
Magnesium
Vit D
Vit K
CoQ10
Shiitake/resihi mushroom
EVOO
Beetroot
Wheatgrass/barley grass
Reservatrol
Alpha-Lipioc acid
Green tea
Berries
Pomegranate
Cruciferous veg
Garlic and onions
Turmeric and ginger
Nuts and seeds

CNM Nut2 S2 Exam revision (9 decks)

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